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Biomedical subjects

M Bianchi

Publications and source records attributed to M Bianchi.

At least 181 records · Page 10Linked to original sources
PubMed1994

Intracerebroventricular interleukin-1 alpha increases immunocyte beta-endorphin concentrations in the rat: involvement of corticotropin-releasing hormone, catecholamines, and serotonin.

The opioid peptide beta-endorphin (BE) is synthesized and secreted by the cells of the immune system and has been shown to participate in the modulation of immune responses, e.g. during stress. Interleukin-1 (IL-1) is a potent activator of the corticotropin-releasing hormone (CRH) system in the hypothalamus, and it has been shown to be involved in many stress responses, including immunosuppression. We studied the effect of centrally injected IL-1 alpha on immunocyte BE concentrations in the rat. IL-1 alpha (1 ng/rat, intracerebroventricularly) significantly (P < 0.01) increased the concentrations of the peptide in splenocytes, lymph node cells, and peripheral blood mononuclear cells 2 and 24 h after treatment. Intracerebroventricular, but not iv, administration of 2 micrograms IL-1 receptor antagonist blocked the IL-1 alpha-induced increase. These effects were also prevented by the intracerebroventricular administration of the CRH receptor antagonist alpha-helical CRH-(9-41). Treatment with 6-hydroxydopamine and 5,7-dihydroxytryptamine, which deplete the catecholaminergic or the serotoninergic systems, respectively, blocked the increase in BE induced by the cytokine. In contrast, hypophysectomy and treatment with indomethacin did not modify the effect of IL. The increase in immunocyte BE, therefore, seems to depend on the activation of CRH, catecholamines, and serotonin, but to be independent of activation of the hypothalamus-pituitary-adrenal-axis and prostaglandins. The immunocyte BE increase could be involved in the immunosuppression induced by central IL-1 alpha.

Adrenalectomy↗
PubMed1994

Bleeding time in preeclampsia.

The association of preeclampsia with thrombocytopenia and prolonged bleeding time is reported. The analysis of bleeding time (Simplate II) and the platelet count (Automatic Coulter Counter) in 41 patients with different grades of preeclampsia is presented. Our results suggest that the decrease in the bleeding time observed in moderate preeclampsia and the increase observed in severe preeclampsia are not mainly dependent on the platelet count.

Adult↗
PubMed1994

Cytokines in acute myocardial infarction: selective increase in circulating tumor necrosis factor, its soluble receptor, and interleukin-1 receptor antagonist.

Cytokines play a pathogenetic role in a variety of infective and inflammatory diseases. In the present study, we had two objectives: (a) to define the kinetics of tumor necrosis factor (TNF) in plasma after acute myocardial infarction (AMI) in patients treated with early thrombolysis, and (b) to measure other cytokines, interleukin-1 (IL-1) and TNF receptor antagonists, in plasma. TNF-alpha, but not IL-1 beta or IL-8, was present in plasma of 6 of 7 patients with severe AMI (Killip class 3 or 4). No TNF (< 50 pg/ml) was detected in a group of 11 patients with uncomplicated myocardial infarction (Killip class 1) or in control patients without AMI. Soluble TNF receptor type I and IL-1 receptor antagonist (IL-1Ra) were also significantly increased in the group with severe AMI compared with those with uncomplicated AMI. Circulating TNF is increased only in AMI complicated by heart failure at hospital admission. This finding may have diagnostic and therapeutic relevance.

Aged↗
PubMed1993

Naloxone-induced analgesia: involvement of kappa-opiate receptors.

Rats treated with an acute high dose (30 mg/kg) or 4 days with a lower dose (5 mg/kg) of naloxone or naltrexone show an analgesic response at the hot-plate test. This paradoxical analgesic effect of the two mu-opiate receptor antagonists is blocked by the kappa opiate receptor antagonist MR 1452, and is modulated by the kappa opiate receptor agonist U 50-488. Our results suggest that kappa opiate receptors are involved in naloxone-induced analgesia and are consistent with a high degree of plasticity of the opiatergic system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1993

Evidence for an opioid inhibitory effect on T cell proliferation.

The proliferative response of human or rat T lymphocytes to phytohemagglutinin (PHA) or concanavalin A (ConA) was measured after acute (30 min) or chronic (8 days) treatment with the opiate receptor antagonists naloxone or naltrexone. Both in the rat and in the human, proliferation was significantly enhanced by acute treatment with the opiate receptor antagonists. In contrast, after chronic treatment proliferation always decreased. The sudden removal of an opioid inhibitory tone might be the basis for the increased proliferative responses observed after acute treatment. The decrease after chronic treatment could be ascribed to the amplification of the inhibitory effect of endogenous opioids due to the up-regulation of opiate receptors that follows chronic antagonist administration. Receptor binding studies of beta-endorphin receptors on splenocytes of chronically naloxone treated rats confirmed this hypothesis: a higher number of beta-endorphin receptors were expressed on splenocytes of naloxone-treated rats compared to controls (Bmax = 9.8 x 10(-12) vs. 1.16 x 10(-12), respectively).

Adult↗
PubMed1993

Peripherally administered IL-1 alpha interferes with scopolamine-induced amnesia in mice.

We studied the effects of human recombinant interleukin-1 alpha on scopolamine-induced amnesia for a passive avoidance response in the mouse. Post-training intraperitoneal administration of the cytokine (0.25 or 0.50 microgram/mouse) significantly reduced the amnesic effect of scopolamine (1.0 mg/kg i.p.). Our results indicate that peripheral interleukin-1 alpha can influence behavior and suggest the involvement of the cholinergic system in the neuromodulatory actions of this cytokine.

Amnesia↗
PubMed1993

Reversal of scopolamine-induced amnesia by the GABAB receptor antagonist CGP 35348 in the mouse.

We studied the effects of CGP 35348, a centrally active blocker of GABAB receptors, on scopolamine-induced amnesia for a passive avoidance response in the mouse. Both pre-training or post-training intraperitoneal administration of the GABAB antagonist (75, 150 and 300 mg/kg i.p.) significantly reduces the amnesic effect of scopolamine (1.0 mg/kg i.p.). Our results are in agreement with previous observations indicating a role for the GABAB receptors in the modulation of memory function, and suggest a possible role of GABAB receptor antagonists as nootropic drugs.

Amnesia↗
PubMed1993

The pneumotoxicant paraquat induces IL-8 mRNA in human mononuclear cells and pulmonary epithelial cells.

Paraquat (PQ) is a herbicide which is highly pneumotoxic by generating reactive oxygen intermediates (ROI). Pro-inflammatory cytokines, particularly IL-1 and TNF, have been implicated in some ROI-mediated pathologies, including bleomycin toxicity and ischaemia/reperfusion injury. We have studied the effect of PQ on the expression of the neutrophil chemotactic cytokine, IL-8, by human peripheral blood mononuclear cells (PBMC). While almost no IL-8 mRNA was detected in unstimulated cells, PQ (100 microM) induced high mRNA expression with a maximum at 24 h of incubation. While PQ did stimulate the appearance of IL-8 mRNA, no significant production of IL-8 protein was detected. However, PQ potentiated the production of IL-8 in the presence of 1 ng/ml of endotoxin (lipopolysaccharide, LPS). This was paralleled by an increased production of chemotactic activity for neutrophils, indicating that the IL-8 was actually bioactive. Stimulation of IL-8 mRNA by PQ was suppressed by IL-4 and by free radical scavengers (dimethylsulfoxide, mannitol). Increased IL-8 expression by PQ was also observed in the human pulmonary epithelial cell line A549 indicating that the effect of PQ was not specific for PBMC. These findings suggest that IL-8 might be involved in the pulmonary effects of PQ and that its production might be stimulated following an oxidative insult, and might clarify the pathogenetic mechanisms of adult respiratory distress syndrome (ARDS) or oxidant-induced pulmonary fibrosis.

Antioxidants↗
PubMed1993

Interleukin-2 enhances scopolamine-induced amnesia and hyperactivity in the mouse.

We studied the effects of human recombinant interleukin-2 (IL-2) on scopolamine-induced amnesia for a passive avoidance response and on scopolamine-induced hyperactivity, in the mouse. The pre-training intraperitoneal administration of the cytokine significantly enhanced the amnesic effect of scopolamine (1.0 mg kg-1 i.p.). Similar effects were observed after repeated administration (2,500 IU/mouse i.p. for 10 days) of the cytokine. In this condition, the treatment with the pro-cholinergic drug acetylcarnitine completely blocked the pro-amnesic effect of IL-2. The cytokine did not affect plasma glucose concentrations, nor induced any change in footshock sensitivity. Intraperitoneal injection of IL-2 significantly enhanced the scopolamine-induced hyperactivity, whereas the cytokine alone was ineffective in modifying locomotor activity. Our results suggest an involvement of the cholinergic system in the neuromodulatory action of IL-2.

Amnesia↗
PubMed1993

Early down-regulation of TNF production by LPS tolerance in human monocytes: comparison with IL-1 beta, IL-6, and IL-8.

We studied the effect of a 4-hr preexposure to LPS on the ability of human monocytes to respond to a subsequent stimulation with LPS in terms of cytokine production. LPS-preexposed monocytes did not produce TNF on LPS restimulation, but they retained the ability to produce IL-1 beta, IL-6, and IL-8. LPS-tolerant monocytes were still capable of producing TNF when restimulated with zymosan. Down-regulation of TNF by LPS tolerance was also evident at the mRNA level. To investigate the possible mechanisms underlying this phenomenon, we also studied the effect of LPS preexposure on membrane CD14, which was suggested to be an LPS receptor, and on intracellular cAMP, an inhibitor of TNF production. LPS induced a 50% decrease in CD14 expression. On the other hand, the increase in cAMP levels by LPS was not affected by preexposure to LPS. In conclusion, (a) TNF is more rapidly down-regulated than IL-1 beta, IL-6, and IL-8 during LPS tolerance in vitro; (b) early LPS tolerance is associated with decreased CD14, which might partially explain the decreased LPS response; and (c) a feedback mechanism controlling TNF synthesis, cAMP elevation, is not down-regulated in LPS tolerance.

Antigens, CD↗
PubMed1993

[Usefulness of GnRH agonists in preoperative treatment of complicated uterine myomata].

The use of long acting gonadotropin-releasing hormone (Gn-RH) agonist produces a reversible hypogonadotropic hypogonadism. This effect has been used as presurgical treatment of uterine myomata, resulting in amenorrhea and reduction in uterus and tumour sizes. We describe the case of a 43 year old patient, having a uterine myoma associated with metrorrhagia, admitted to hospital because of extensive deep phlebothrombosis requiring urgent anticoagulation. Because of the risk of exacerbating metrorrhagia and considering the high morbidity associated to emergency hysterectomy, we decided medical treatment with a depot GnRH agonist (leuprolide acetate 3.75 mg IM monthly). Bleeding ceased within 3 days, allowing the maintenance of anticoagulant treatment. A marked reduction in uterine size postponed total hysterectomy to 3 months later. The characteristics of GnRH analogues, their action mechanisms, adverse effects and other clinical indications are discussed.

Adult↗
PubMed1993

Glomerular permselectivity to macromolecules in reflux nephropathy: microalbuminuria during acute hyperfiltration due to aminoacid infusion.

Reflux nephropathy is an important cause of chronic renal failure in children. After the parenchymal scar, the progression is thought to be mediated by glomerular hypertension in remnant nephrons resulting in modifications in permselectivity to macromolecules. Proteinuria correlates with a progressive course. The glomerular permselectivity to macromolecules in basal conditions and after acute hemodynamic stress was investigated in 28 children whose bilateral vesico-ureteric reflux (VUR) had been previously surgically corrected (meanly 5.6 years before) and with normal creatinine clearance (CrCl). Bilateral renal scarring (0 to 8 scale for both kidneys) was 4.3 +/- 1.6. Albuminuria (UAE) was evaluated in basal conditions and under acute hyperfiltration induced by amino acid (Aa) infusion. After isotonic saline at 310 ml/hour/1.73 m2, 6 mg/kg/min of Aa were infused for 2 hrs. UAE was significantly higher than controls in basal conditions (p < 0.01), and further increased after Aa infusion (p < 0.02). Microalbuminuria was detectable in 53.5% of the children in basal conditions and in 64.3% after Aa. Also urinary beta 2 microglobulin significantly increased at the end of the test (p < 0.001). CrCl significantly increased at the first hour (p < 0.05). Children with severe renal parenchymal scarring had greater UAE (p < 0.01) and beta 2M (p < 0.02) values after provocative test than those with mild renal damage. In 8 children GFR and ERPF were measured by means of inulin and p-hippurate clearance respectively. The variations in UAE during Aa infusion were significantly correlated with GFR dynamics (p < 0.05) while they were not influenced by ERPF modifications.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMed1993

Suppression of interleukin-6 production in endotoxin tolerance in a mouse glioma cell line: reversal by phorbol ester.

Tolerance to endotoxin (lipopolysaccharide, LPS) was shown to be mediated by an inhibition of cytokine production. We have studied the effect of 3-day pretreatment with LPS on production of IL-6 in response to a subsequent challenge with LPS in a mouse glioma. The results indicated that in this model, a complete blockage of IL-6 production is induced by LPS pretreatment. This is associated with a decrease of LPS-induced IL-6 mRNA levels. LPS-induced IL-6 production can be restored by PMA, as it was previously observed in vivo, suggesting that down-regulation of IL-6 response in LPS tolerance occurs at the transcriptional level, probably by down-regulating protein kinase C or some other PMA-activable signaling system. IL-6 production is also down-regulated by 3-day preincubation with IL-6 and, to a lesser extent, with IL-1 or TNF, indicating that IL-6 can down-regulate its own production.

Animals↗
PubMed1993

Cryptococcosis produced by a urease negative strain of Cryptococcus neoformans.

A urease negative strain of Cryptococcus neoformans was isolated form a patient with AIDS. The identification of the yeast was confirmed by physiological and pathogenicity tests. Clinically, the disseminated cryptococcal infection in our patient was identical to those reported in other patients with AIDS.

AIDS-Related Opportunistic Infections↗
PubMed1993

Surgical treatment of arthritic valgus knee: femoral supracondylar osteotomy or knee replacement?

Twenty-two of the 24 patients operated on with femoral supracondylar osteotomy for arthritic valgus knee between 1978 and 1987 were evaluated, comparing the results with those obtained in a similar group of 10 patients with the same disorder treated with knee replacement during the same period. From a functional viewpoint and according to the Hospital for Special Surgery rating scale, the results of the osteotomy were not significantly different from the extremely positive outcome of the knee replacement. However, as far as pain is concerned, only 50% of the osteotomy patients were completely asymptomatic after the operation. In the 50% of the osteotomy patients with post-operative under or over correction of the mechanical axis of the knee, the results were unsatisfactory. Finally, there was only one case of delayed union. In the light of these results, in contrast to what has been said by other authors, femoral osteotomy may be considered a valid alternative to knee replacement in the treatment of arthritic valgus knee in active subjects, less than 65 years old, with a valgus angulation of no more than 15 degrees and Ahlback stage 2 beta arthritis of the lateral compartment. It is, however, a technique which requires extreme precision both in planning and performing the operation.

Adult↗
PubMed1992

Central effects of tumor necrosis factor alpha and interleukin-1 alpha on nociceptive thresholds and spontaneous locomotor activity.

To extend the knowledge on the central effects of cytokines, we studied the effects of tumor necrosis factor alpha and interleukin-1 alpha on nociceptive thresholds and spontaneous locomotor activity in rats. After central administration, both tumor necrosis factor alpha and interleukin-1 alpha significantly (P < 0.001) increase the nociceptive thresholds as measured by the hot-plate test. Tumor necrosis factor alpha, but not interleukin-1 alpha decreases spontaneous locomotor activity evaluated by the Animex test. The increase in nociceptive thresholds induced by tumor necrosis factor alpha or interleukin-1 alpha is not affected by the opiate receptor antagonist naloxone, or antisera against the endogenous opioids beta-endorphin, met-enkephalin or dynorphin. The analgesic effect of tumor necrosis factor alpha is completely antagonized by anti-IL-1 antibodies. Moreover, the cyclooxygenase inhibitor indomethacin does not antagonize the increase of nociceptive thresholds induced by either cytokine.

Analgesia↗